Regeneration following tissue necrosis is mediated by non-apoptotic caspase activity.

Tissue necrosis is a devastating complication for many human diseases and injuries. Unfortunately, our understanding of necrosis and how it impacts surrounding healthy tissue - an essential consideration when developing effective methods to treat such injuries - has been limited by a lack of robust genetically tractable models. Our lab previously established a method to study necrosis-induced regeneration in the wing imaginal disc, which revealed a unique phenomenon whereby cells at a distance from the injury upregulate caspase activity in a process called Necrosis-induced Apoptosis (NiA) that is vital for regeneration.

Necrosis-induced apoptosis promotes regeneration in Drosophila wing imaginal discs.

Regeneration is a complex process that requires a coordinated genetic response to tissue loss. Signals from dying cells are crucial to this process and are best understood in the context of regeneration following programmed cell death, like apoptosis. Conversely, regeneration following unregulated forms of death, such as necrosis, have yet to be fully explored.

Characterization of a novel pathogenic variant in the gene associated with erythropoietic protoporphyria.

Erythropoietic protoporphyria (EPP) is an autosomal recessive deficiency in heme biosynthesis due to pathogenic variants in the ferrochelatase gene (). Patients present with lifelong photosensitivity and potential liver disease. Here we report a novel variant designated c.